AIM: To determine whether high-protein, high-fat, and low-carbohydrate diets can cause lesions in rat livers.METHODS: We randomly divided 20 female Wistar rats into a control diet group and an experimental diet group....AIM: To determine whether high-protein, high-fat, and low-carbohydrate diets can cause lesions in rat livers.METHODS: We randomly divided 20 female Wistar rats into a control diet group and an experimental diet group. Animals in the control group received an AIN-93 M diet, and animals in the experimental group received an Atkins-based diet(59.46% protein, 31.77% fat, and 8.77% carbohydrate). After 8 wk, the rats were anesthetized and exsanguinated for transaminases analysis, and their livers were removed for flow cytometry, immunohistochemistry, and light microscopy studies. We expressed the data as mean ± standard deviation(sd) assuming unpaired and parametric data; we analyzed differences using the student's t-test. statistical significance was set at P < 0.05.RESULTS: We found that plasma alanine aminotransferase and aspartate aminotransferase levels were significantly higher in the experimental group than in the control group. According to flow cytometry, the percentages of nonviable cells were 11.67% ± 1.12% for early apoptosis, 12.07% ± 1.11% for late apoptosis, and 7.11% ± 0.44% for non-apoptotic death in the experimental diet group and 3.73% ± 0.50% for early apoptosis, 5.67% ± 0.72% for late apoptosis, and 3.82% ± 0.28% for non-apoptotic death in the control diet group. The mean percentage of early apoptosis was higher in the experimental diet group than in the control diet group. Immunohistochemistry for autophagy was negative in both groups. sinusoidal dilation around the central vein and small hepatocytes was only observed in the experimental diet group, and fibrosis was not identified by hematoxylin-eosin or Trichrome Masson staining in either group.CONCLUSION: Eight weeks of an experimental diet resulted in cellular and histopathological lesions in rat livers. Apoptosis was our principal finding; elevated plasma transaminases demonstrate hepatic lesions.展开更多
Objective: Idiopathic reactive hypoglycemia is defined as early postprandial hypoglycemia occurring on ingestion of high carbohydrate containing meal. Remission ensues with high protein low carbohydrate diet. This stu...Objective: Idiopathic reactive hypoglycemia is defined as early postprandial hypoglycemia occurring on ingestion of high carbohydrate containing meal. Remission ensues with high protein low carbohydrate diet. This study assessed roles of insulin and glucagon in its onset and remission. Methods: Plasma glucose, insulin and glucagon were determined after an overnight fast and repeatedly until 180 minutes on ingestion of 3 meals;100 g glucose;100 g pure protein liquid and mixture of 50 g each at 14 days’ interval. Five adults with IRH and 6 age matched healthy volunteers participated. Results: In IRH, glucose ingestion induced prompt rise in glucose (5.1 ± 0.8 to10.5 ± 1.2 mM/L) followed later by hypoglycemia (2.6 ± 0.4 mM/L). Insulin rose from 7 ± 2 to 90 ± 18 mU/L. Glucagon rose initially (10% ± 2%) from elevated basal concentration (373 ± 57 mU/L) followed by later decline (-43% ± 12%). On protein ingestion, glucose declined followed by a restoration to basal level while both insulin and glucagon rose (28 ± 6 mU/L;148% ± 38%, p < 0.01). However, insulin response was lower and glucagon rise was greater when compared to responses on glucose ingestion (p < 0.01). With mixed meal, glucose (8.2 ± 0.6 mM/L), insulin (65 ± 12 mU/L) and glucagon (48% ± 7%) responses were lesser than rises following glucose ingestion (p < 0.05) and hypoglycemia did not occur. Conclusion: In IRH, initial hyperglycemia on glucose ingestion may be exacerbated by paradoxical glucagon rise and hypoglycemia may be induced by increased insulin and declining glucagon responses. Resolution of hypoglycemia with high protein low carbohydrate diet may be attributed to blunting of insulin response and concurrent glucagon rise.展开更多
BACKGROUND Reduced level of physical activity,high-fat diet and skeletal muscle atrophy are key factors that are likely to contribute to deleterious changes in body composition and metabolic following spinal cord inju...BACKGROUND Reduced level of physical activity,high-fat diet and skeletal muscle atrophy are key factors that are likely to contribute to deleterious changes in body composition and metabolic following spinal cord injury (SCI).Reduced caloric intake with lowering percentage macronutrients of fat and increasing protein intake may likely to improve body composition parameters and decrease ectopic adiposity after SCI.AIM To highlight the effects of dietary manipulation and testosterone replacement therapy (TRT) on body composition after SCI METHODS A 31-year-old male with T5 SCI was administered transdermal TRT daily for 16 wk.Caloric intake and percentage macronutrients were analyzed using dietary recalls.Magnetic resonance imaging and dual-energy x-ray absorptiometry were used to measure changes in body composition.RESULTS Caloric intake and fat percentage were reduced by 445 kcal/d and 6.5%,respectively.Total body weight decreased by 8%,body fat decreased by 29%,and lean mass increased by 7%.Thigh subcutaneous adipose tissue cross-sectional area was reduced by 31%.CONCLUSION Manipulation of caloric intake,fat percentage,and protein percentage may have influenced body composition after SCI.展开更多
This review will examine topical issues in weight loss and weight maintenance in people with and without diabetes. A high protein, low glycemic index diet would appear to be best for 12-mo weight maintenance in people...This review will examine topical issues in weight loss and weight maintenance in people with and without diabetes. A high protein, low glycemic index diet would appear to be best for 12-mo weight maintenance in people without type 2 diabetes. This dietary pattern is currently beingexplored in a large prevention of diabetes intervention. Intermittent energy restriction is useful but no better than daily energy restriction but there needs to be larger and longer term trials performed. There appears to be no evidence that intermittent fasting or intermittent severe energy restriction has a metabolic benefit beyond the weight loss produced and does not spare lean mass compared with daily energy restriction. Meal replacements are useful and can produce weight loss similar to or better than food restriction alone. Very low calorie diets can produce weight loss of 11-16 kg at 12 mo with persistent weight loss of 1-2 kg at 4-6 years with a very wide variation in long term results. Long term medication or meal replacement support can produce more sustained weight loss. In type 2 diabetes very low carbohydrate diets are strongly recommended by some groups but the long term evidence is very limited and no published trial is longer than 12 mo. Although obesity is strongly genetically based the microbiome may play a small role but human evidence is currently very limited.展开更多
目的本研究旨在观察高脂饮食联合链脲佐菌素诱导的糖尿病大鼠糖脂代谢指标及肠道菌群结构的变化,以及低脂饮食对其干预的影响。方法实验分别将普通饮食和高脂饮食喂养的大鼠作为对照组和模型组,对其进行8W的低脂饮食干预。实验在开始前...目的本研究旨在观察高脂饮食联合链脲佐菌素诱导的糖尿病大鼠糖脂代谢指标及肠道菌群结构的变化,以及低脂饮食对其干预的影响。方法实验分别将普通饮食和高脂饮食喂养的大鼠作为对照组和模型组,对其进行8W的低脂饮食干预。实验在开始前、后记录所有大鼠体重,取大鼠眼眶血检测糖脂代谢指标,留取大鼠粪便进行肠道微生物多样性检测。结果实验组在低脂饮食干预后,体重、低密度脂蛋白胆固醇(Low Density Lipoprotein Cholesterol,LDL-C)下降明显,差异具有统计学意义(P<0.05),其余指标差异无统计学意义(P>0.05)。糖尿病大鼠中拟杆菌门、放线菌门升高,在低脂饮食控制后TM7及厚壁菌门/拟杆菌门比例显著升高。糖尿病大鼠的关键菌属为普雷沃菌属和拟杆菌属,在低脂饮食干预后,变为瘤胃球菌和梭菌属。低脂饮食干预的关键通路是脂多糖生物合成、糖胺聚糖降解、其他聚糖降解和鞘脂代谢。结论低脂饮食可显著降低糖尿病大鼠体重,改变肠道菌群结构。低脂饮食可能通过改变肠道脂肪代谢通路干预糖尿病的进展。展开更多
文摘AIM: To determine whether high-protein, high-fat, and low-carbohydrate diets can cause lesions in rat livers.METHODS: We randomly divided 20 female Wistar rats into a control diet group and an experimental diet group. Animals in the control group received an AIN-93 M diet, and animals in the experimental group received an Atkins-based diet(59.46% protein, 31.77% fat, and 8.77% carbohydrate). After 8 wk, the rats were anesthetized and exsanguinated for transaminases analysis, and their livers were removed for flow cytometry, immunohistochemistry, and light microscopy studies. We expressed the data as mean ± standard deviation(sd) assuming unpaired and parametric data; we analyzed differences using the student's t-test. statistical significance was set at P < 0.05.RESULTS: We found that plasma alanine aminotransferase and aspartate aminotransferase levels were significantly higher in the experimental group than in the control group. According to flow cytometry, the percentages of nonviable cells were 11.67% ± 1.12% for early apoptosis, 12.07% ± 1.11% for late apoptosis, and 7.11% ± 0.44% for non-apoptotic death in the experimental diet group and 3.73% ± 0.50% for early apoptosis, 5.67% ± 0.72% for late apoptosis, and 3.82% ± 0.28% for non-apoptotic death in the control diet group. The mean percentage of early apoptosis was higher in the experimental diet group than in the control diet group. Immunohistochemistry for autophagy was negative in both groups. sinusoidal dilation around the central vein and small hepatocytes was only observed in the experimental diet group, and fibrosis was not identified by hematoxylin-eosin or Trichrome Masson staining in either group.CONCLUSION: Eight weeks of an experimental diet resulted in cellular and histopathological lesions in rat livers. Apoptosis was our principal finding; elevated plasma transaminases demonstrate hepatic lesions.
文摘Objective: Idiopathic reactive hypoglycemia is defined as early postprandial hypoglycemia occurring on ingestion of high carbohydrate containing meal. Remission ensues with high protein low carbohydrate diet. This study assessed roles of insulin and glucagon in its onset and remission. Methods: Plasma glucose, insulin and glucagon were determined after an overnight fast and repeatedly until 180 minutes on ingestion of 3 meals;100 g glucose;100 g pure protein liquid and mixture of 50 g each at 14 days’ interval. Five adults with IRH and 6 age matched healthy volunteers participated. Results: In IRH, glucose ingestion induced prompt rise in glucose (5.1 ± 0.8 to10.5 ± 1.2 mM/L) followed later by hypoglycemia (2.6 ± 0.4 mM/L). Insulin rose from 7 ± 2 to 90 ± 18 mU/L. Glucagon rose initially (10% ± 2%) from elevated basal concentration (373 ± 57 mU/L) followed by later decline (-43% ± 12%). On protein ingestion, glucose declined followed by a restoration to basal level while both insulin and glucagon rose (28 ± 6 mU/L;148% ± 38%, p < 0.01). However, insulin response was lower and glucagon rise was greater when compared to responses on glucose ingestion (p < 0.01). With mixed meal, glucose (8.2 ± 0.6 mM/L), insulin (65 ± 12 mU/L) and glucagon (48% ± 7%) responses were lesser than rises following glucose ingestion (p < 0.05) and hypoglycemia did not occur. Conclusion: In IRH, initial hyperglycemia on glucose ingestion may be exacerbated by paradoxical glucagon rise and hypoglycemia may be induced by increased insulin and declining glucagon responses. Resolution of hypoglycemia with high protein low carbohydrate diet may be attributed to blunting of insulin response and concurrent glucagon rise.
基金Supported by Department of Veteran Affairs,Veteran Health Administration,Rehabilitation Research and Development Service,No.1IK2RX000732-01A1
文摘BACKGROUND Reduced level of physical activity,high-fat diet and skeletal muscle atrophy are key factors that are likely to contribute to deleterious changes in body composition and metabolic following spinal cord injury (SCI).Reduced caloric intake with lowering percentage macronutrients of fat and increasing protein intake may likely to improve body composition parameters and decrease ectopic adiposity after SCI.AIM To highlight the effects of dietary manipulation and testosterone replacement therapy (TRT) on body composition after SCI METHODS A 31-year-old male with T5 SCI was administered transdermal TRT daily for 16 wk.Caloric intake and percentage macronutrients were analyzed using dietary recalls.Magnetic resonance imaging and dual-energy x-ray absorptiometry were used to measure changes in body composition.RESULTS Caloric intake and fat percentage were reduced by 445 kcal/d and 6.5%,respectively.Total body weight decreased by 8%,body fat decreased by 29%,and lean mass increased by 7%.Thigh subcutaneous adipose tissue cross-sectional area was reduced by 31%.CONCLUSION Manipulation of caloric intake,fat percentage,and protein percentage may have influenced body composition after SCI.
文摘This review will examine topical issues in weight loss and weight maintenance in people with and without diabetes. A high protein, low glycemic index diet would appear to be best for 12-mo weight maintenance in people without type 2 diabetes. This dietary pattern is currently beingexplored in a large prevention of diabetes intervention. Intermittent energy restriction is useful but no better than daily energy restriction but there needs to be larger and longer term trials performed. There appears to be no evidence that intermittent fasting or intermittent severe energy restriction has a metabolic benefit beyond the weight loss produced and does not spare lean mass compared with daily energy restriction. Meal replacements are useful and can produce weight loss similar to or better than food restriction alone. Very low calorie diets can produce weight loss of 11-16 kg at 12 mo with persistent weight loss of 1-2 kg at 4-6 years with a very wide variation in long term results. Long term medication or meal replacement support can produce more sustained weight loss. In type 2 diabetes very low carbohydrate diets are strongly recommended by some groups but the long term evidence is very limited and no published trial is longer than 12 mo. Although obesity is strongly genetically based the microbiome may play a small role but human evidence is currently very limited.
文摘目的本研究旨在观察高脂饮食联合链脲佐菌素诱导的糖尿病大鼠糖脂代谢指标及肠道菌群结构的变化,以及低脂饮食对其干预的影响。方法实验分别将普通饮食和高脂饮食喂养的大鼠作为对照组和模型组,对其进行8W的低脂饮食干预。实验在开始前、后记录所有大鼠体重,取大鼠眼眶血检测糖脂代谢指标,留取大鼠粪便进行肠道微生物多样性检测。结果实验组在低脂饮食干预后,体重、低密度脂蛋白胆固醇(Low Density Lipoprotein Cholesterol,LDL-C)下降明显,差异具有统计学意义(P<0.05),其余指标差异无统计学意义(P>0.05)。糖尿病大鼠中拟杆菌门、放线菌门升高,在低脂饮食控制后TM7及厚壁菌门/拟杆菌门比例显著升高。糖尿病大鼠的关键菌属为普雷沃菌属和拟杆菌属,在低脂饮食干预后,变为瘤胃球菌和梭菌属。低脂饮食干预的关键通路是脂多糖生物合成、糖胺聚糖降解、其他聚糖降解和鞘脂代谢。结论低脂饮食可显著降低糖尿病大鼠体重,改变肠道菌群结构。低脂饮食可能通过改变肠道脂肪代谢通路干预糖尿病的进展。
